Abscess formation will cause nerve impingement findings with fever Cellulitis is easily found by external exam Accidental dural puncture causes headaches that are positional Injection site pain is minimal (but for many complex pain patients...nothing is minimal)

Realistically there is no true complications from the needle "hitting a nerve". It is within the realm of possibilities, but much like bigfoot, it is reported by dubious individuals with extraordinary stories.

Dr. Wagner, I am a clinical instructor who is quite involved teaching differential diagnosis to PT students because of the need of the environment I am employed. In PT school, our ddx course was neither practical nor efficient, and based on what current students are telling me now, not much has changed. Therefore I've been shopping for different approaches to this topic. Currently I use the VINDICATE model have my students (quickly) recite as many possibilities from most to least likely (including non-neuromuskuloskeletal causes) so they can learn to be aware of competing diagnosis, so the patient can be referred back if necessary. Do you have any suggestions? Did you learn using VINDICATE? or is there a different approach I should consider.

(sidenote: do you teach or would you consider teaching ddx process to PTs??)

I did not learn differential diagnosis with any specific model. In medical school there are MANY overlapping classes that teach differential diagnosis...from pathology to the clinical sciences (internal medicine, surgery, OBGYN, peds, EM etc). It pretty much is non stop differential diagnosis. Many schools use group learning to discuss topics and sometimes that is helpful. But the most effective way for me was pounding it into my head, then seeing it.

Example: Shortness of breath. The differential is gigantic. Discussing the the case and then seeing the pathology creates patterns. It is hard, but that is what physicians do...differential diagnosis. I do differential diagnosis very quickly as it is part of my job...I also quickly differentiate deadly vs non deadly pathologies...that is my primary goal. I may not be able to tell you WHY your chest hurts, but is NOT pneumonia, it is NOT a heart attack, it is NOT esophogeal rupture, it is NOT a pulmonary embolus, it is NOT a pneumothorax...

I had a pt a few months ago whose MOI was getting box out of her car and hitting the back of her head on the roof. She had a C-scan and X-rays and was told that just had a mild concussion and cervical strain. When I performed some manual cervical traction in supine she became SOB, I released the SOB immediately resolved and I asked her if I was hurting her and and she said "no it just felt like I couldn't breathe" so I tried again this time applying the traction force more slowly and in a graded fashion and the same thing happened so I tried other things: NAGs, SNAGs, sideglide mobilizations and soft tissue stuff she tolerated all these quite well. I tried the manual traction again on a subsequent visit and got the same result and stuck to other methods after that.

What could be causing this? Should the referring physician have been notified? Has anyone else had a pt with this experience?

At first I thought anxiety slash just not being comfortable, but I really didn't get that impression. She is long discharged now and back to semi-competive rowing, I documented her response, but is this something I should have been in contact with referring physician about?

It comes down to this, if you would/could/did have a hard time forgetting the case while at home or driving home, then you should have made the call. Ultimately YOU need to feel at ease. While the referring doc likely would have just noted the reaction, sometimes phone calls are about "covering the bases".

What are your thoughts on whether an azygous lobe could cause symptoms, and what symptoms this might cause?

I have seen a young woman 30 y.o. with neck and mid back pain, but also with atypical symptoms such as inability to tolerate aerobic exercise due to perceived trouble breathing and tightness sensation in her throat if she tries to run. She was referred due to symptoms that seemed mostly related to mechanical neck pain, with UE paresthesias, numbness/tingling in hands with driving, but she also noted the aforementioned issues with exercise. She felt arm and leg weakness, but by muscle tests had nothing profound, just slight weakness in lower traps and rhomboids at 4/5 and faster onset of fatigue with the right arm relative to the left. She also described hand stiffness and occasional (1-2x per week) shooting pain in her legs OR her arms, of transient nature, often while walking. Neuro workup for MS and the like was negative, and an EMG was negative as well. Chest films showed the incidental finding of an azygous lobe. Certainly some of her symptoms are mechanical in nature, but not all.

I really doubt that would be the cause, the lung is so compliant...of course a mass that was in the lung and taking up space CERTAINLY would cause symptoms (ie Pancoast tumor...which is not compliant)...good idea for a case eh?

It states: " In conclusion, the quest to understand type 1 diabetes has largely been driven by the mechanistic approach, which has striven to characterize the disease in terms of defining molecular abnormalities. This goal has proved elusive[74]. Given the complexity and diversity of biological systems, it seems increasingly likely that the mechanistic approach will need to be supplemented by a more ecological concept of balanced competition between complex biological processes, a dynamic interaction with more than one possible outcome. The traditional antithesis between genes and environment assumed that genes were hardwired into the phenotype, whereas growth and early adaptation to the environment are now viewed as an interactive process in which early experience of the outside world is fed back to determine lasting patterns of gene expression. The biological signature of each individual thus derives from a dynamic process of adaptation, a process with a history. RenÚ Dubos[75] expressed this many years ago when he stated that "socially and individually the response of human beings to the conditions of the present is always conditioned by the biological remembrance of things past." We are indeed part of all that we have met. The implications of the changing demography of type 1 diabetes for our understanding of the disease are considerable. From the point of view of the geneticist, it means that patterns of inheritance that confer susceptibility to immune-mediated loss of pancreatic ▀-cells became progressively maladaptive in a late 20th century environment. For the immunologist, it implies that the ontogeny of the immune response in early childhood is changing in such a way that potentially harmful responses are now more prevalent, or more aggressive, in the subpopulation of genetically susceptible children. The task for the epidemiologist is to explain this. For the clinician, it means that childhood diabetes was in the past a partly preventable condition, and could become so again."

Thank you, Dr. Wagner for your earlier reply to the differential diagnosis education question. I think you would do a great job teaching a ddx class to PTs--especially with your 'dual credentialed' background!

Second question: If you have a patient you suspect is having an acute CVA in the posterior fossa/cerebellar territory--do you still order a head CT first, or can you jump to doing an MRI/MRA? I do understand if you want to catch a hemorrhage early on, the CT is fine for visualizing this (along with a limited differential), but isn't this a difficult area of the brain to view using CT imaging, and how well will CT show an acute ischemic event?

I have encountered this dilemma several times in practice, and the docs I work with respond with "it's protocol" and "the neuro team will want a head CT first anyway". It's almost as if their hands are tied.. maybe they are? What else goes into this decision tree? I imagine its a time, money, flow, thing, but I would really value a candid answer. Also, is there any particular way of phrasing a verbal report to trigger MRI/MRA instead of CT first? Given it is often inevitably read as 'neg. acute', but examining the patient suggests otherwise.

A CT is fast efficient and easy to do. In the face of acute neurologic deficit you want to DISPROVE hemorrhage. A CT is the test of choice for this in the acute phase. And while Ischemic neurologic changes far outnumber hemorrhagic neurologic changes...you certainly do not want to use a thrombolytic on any but the absolute correct patient. The CT is the best way to evaluate (quickly) the best patient (you have 4 hours from time of onset).

I get updates daily through numerous sources...but I generally prescribe old school meds. I don't get too fancy EVER (my patients are poor, and new fancy meds are for PCP's that get drug reps on a daily basis...suckers)

CT's miss about 5% of SAH. Usually these patients suffer from hypertensive bleeds, which often times prevent thrombolytics anyway if one would be considering the option in the face of possible ischemia. No one likes pushing thrombolytics.